Metabolic regulation in erythroid differentiation by systemic ketogenesis in fasted mice
Red blood cells (RBCs) formation from progenitor cells in bone marrow (BM) requires enormous energy supply through a stepwise metabolic switch from oxidative phosphorylation to glycolysis during erythropoiesis 1,2. Glucose and glutamine act as the principal nutrient source for nucleotide biosynthesis to regulate the commitment of human and murine hematopoietic stem cells (HSCs) to the erythroid lineage 3. It was reported that control of erythroid differentiation and maturation is also fine-tuned by fatty acids and cholesterol through the regulation of metabolic shift 4,5. (Source: Experimental Hematology)
Source: Experimental Hematology - October 25, 2023 Category: Hematology Authors: Wenjuan Ma, Yuichiro Arima, Terumasa Umemoto, Tomomasa Yokomizo, Yuqing Xu, Kenichi Miharada, Yosuke Tanaka, Toshio Suda Tags: Article Source Type: research
MiR-223-3p promotes genomic stability of hematopoietic progenitors after radiation
Most ionizing radiation (IR) DNA damage is repaired by the classical non-homologous end-joining (cNHEJ) or the conservative homologous recombination (HR) pathway; however, when damage is extensive, a back-up pathway termed alternative non-homologous end joining (aNHEJ) is activated [1 –3]. The rate limiting step in aNHEJ is when PARP1 successfully competes with the Ku complex for a free DNA end of a double-strand break (DSB) [4]. While aNHEJ can rapidly repair DSBs, this mechanism often results in deletions at the site of end-joining due to trimming of overhanging DNA strands a fter microhomology annealing [4]. (Source: ...
Source: Experimental Hematology - October 22, 2023 Category: Hematology Authors: Shi Chen, Gayathri Srinivasan, Aruna Jaiswal, Elizabeth A. Williamson, Lingxiao Li, Dominic Arris, Daohong Zhou, Mingjiang Xu, Robert Hromas Tags: Brief Communication Source Type: research
MiR223-3p Promotes Genomic Stability of Hematopoietic Progenitors After Radiation
Most ionizing radiation (IR) DNA damage is repaired by the classical non-homologous end-joining (cNHEJ) or the conservative homologous recombination (HR) pathway, but when damage is extensive, a back-up pathway termed alternative Non-Homologous End Joining (aNHEJ) is activated (1-3). The rate limiting step in aNHEJ is when PARP1 successfully competes with the Ku complex for a free DNA end of a double strand break (DSB) (4). While aNHEJ can rapidly repair DSBs, this mechanism often results in deletions at the site of end-joining due to trimming of overhanging DNA strands after microhomology annealing (4). (Source: Experimental Hematology)
Source: Experimental Hematology - October 22, 2023 Category: Hematology Authors: Shi Chen, Gayathri Srinivasan, Aruna Jaiswal, Elizabeth A. Williamson, Lingxiao Li, Dominic Arris, Daohong Zhou, Mingjiang Xu, Robert Hromas Tags: Brief Communication Source Type: research
The multifaceted role of mitochondria in HSC fate decisions: energy and beyond
Hematopoietic stem cells are at the apex of the hematopoietic hierarchy. Multipotent by nature, they have the potential to differentiate into all mature hematopoietic lineages to replenish the blood system, at steady state or under stress conditions. HSCs mostly reside in a quiescent state to prevent their premature exhaustion due to replicative stress. They divide from time to time to produce highly proliferative progenitors that commit to differentiation, and daughter HSCs that return to a quiescent state in order to maintain stemness characteristics, known as self-renewal. (Source: Experimental Hematology)
Source: Experimental Hematology - October 11, 2023 Category: Hematology Authors: Marie-Dominique Filippi Tags: Review Source Type: research
How Nutrition Regulates Hematopoietic Stem Cell Features
Throughout life, hematopoiesis guarantees an adequate supply of blood cells. Hematopoietic stem cells (HSCs) sit at the apex of the hematopoietic system and hold the unique ability to self-renew and replenish all blood cell types. As HSCs differentiate, they give rise to progenitor cells with restricted potency that will undergo further differentiation and maturation, eventually producing fully functional blood cells. Adult HSCs typically reside in a deep state of quiescence to prevent DNA damage and the depletion of the stem cell pool from excessive cell divisions1,2. (Source: Experimental Hematology)
Source: Experimental Hematology - October 7, 2023 Category: Hematology Authors: Katharina Sch önberger, Nina Cabezas-Wallscheid Tags: Review Source Type: research
MiR-455-3p mediates PPAR α through UBN2 to promote apoptosis and autophagy in acute myeloid leukemia cells
Acute myeloid leukemia (AML) is a hackneyed type of acute leukemia that is a highly specific, invasive, and rare tumor[1-3]. Its characteristics are aberrant proliferation of original or immature cells in blood, bone marrow and other tissues, stasis of differentiation, and dysfunction of cell apoptosis, leading to restraint of normal hematopoietic function[4]. At present, the first-line remedy for AML is chiefly based on combination chemotherapy and stem cell transplantation. Despite significant progress in AML treatment, the overall survival rate is still low [2, 5]. (Source: Experimental Hematology)
Source: Experimental Hematology - October 4, 2023 Category: Hematology Authors: Yu Xie, Lin Tan, Kun Wu, Deyun Li, Chengping Li Tags: Article Source Type: research
Metabolic Regulation of Aged Hematopoietic Stem Cells: Key Players and Mechanisms
The process of aging is a complex phenomenon that affects nearly all tissues and biological systems and exerts a profound influence on the functionality and metabolic processes of hematopoietic stem cells (HSCs), which are responsible for the maintenance of lifelong generation of all blood cell types. With age, HSCs show impaired regenerative potential and increase their metabolic activity, which is associated with an increased expansion of the stem cell pool and accompanied by skewing of differentiation towards the myeloid lineage. (Source: Experimental Hematology)
Source: Experimental Hematology - September 29, 2023 Category: Hematology Authors: Nazanin Karimnia, James Harris, Shen Y. Heazlewood, Benjamin Cao, Susan K. Nilsson Tags: Review Source Type: research
Inhibition of PAK1 generates an ameliorative effect on MPLW515L mouse model of myeloproliferative neoplasms by regulating the differentiation and survival of the megakaryocytes
Classical myeloproliferative neoplasms (MPNs) are clonal haematological disorders that result in the overproduction of cells derived from the myeloid lineage [1]. A new diagnostic approach classifies MPN into three types: polycythemia vera (PV), essential thrombocythemia (ET), and primary myelofibrosis (PMF). These three types of myelofibrosis can progress to post-PV or ET myelofibrosis (PPV-MF and PET-MF, respectively) [2,3]. MPNs are characterized by bone marrow reticulin/collagen fibrosis, aberrant inflammatory cytokine expression, hepatosplenomegaly, extramedullary leukemic progression, and shortened survival [4]. (Sou...
Source: Experimental Hematology - September 21, 2023 Category: Hematology Authors: Chunling Fu, Xueting Hu, Shujin Wang, Xiangru Yu, Qigang Zhang, Liwei Zhang, Kunming Qi, Zhenyu Li, Kailin Xu Source Type: research
Microenvironment in Acute Myeloid Leukemia: focus on senescence mechanisms, therapeutic interactions and future directions
Acute myeloid leukemia (AML) is a group of hematologic malignancies characterized by differentiation impairment and clonal proliferation of hematopoietic progenitors. AML affects mainly older adults (median age of onset>65 years 1,2), and includes entities characterized by peculiar clinical features and different response to treatment. (Source: Experimental Hematology)
Source: Experimental Hematology - September 21, 2023 Category: Hematology Authors: Luca Guarnera, Enrico Santinelli, Elisa Galossi, Antonio Cristiano, Emiliano Fabiani, Giulia Falconi, Maria Teresa Voso Tags: Review Source Type: research
Genetic Mutation Signature for Relapse Prediction in Normal Karyotype Acute Myeloid Leukemia
Acute myeloid leukemia (AML) is a highly heterogeneous disease with a poor prognosis, largely owing to its high incidence of relapse1-3. Normal karyotype (NK-AML) is observed in nearly half of AML cases4. The identification of specific genetic mutations has remarkably augmented our understanding of AML molecular pathophysiology and revealed the prognostic significance of each mutation in NK-AML5-7. The classification of AML and its prognostic profile have been improved owing to advances in molecular characterization and the application of high-throughput sequencing. (Source: Experimental Hematology)
Source: Experimental Hematology - September 19, 2023 Category: Hematology Authors: Lijie Han, Jiaying Wu, Xiaodong Lyu, Jifeng Yu, Xiaolin Han, Hongmian Zhao, Zhilei Bian, Wei Li, Wenjuan Fan, Chen He, Weimin Wang, Mengmeng Zhang, Yafei Li, Chao Liu, Hui Sun, Haixia Cao, Li'na Sang, Jun Zhang, Zhongxing Jiang, Jie Peng Source Type: research
Physiological and regenerative functions of sterile- α motif protein-14 in hematopoiesis
Samd14 promotes signal pathway duration and intensity in hematopoietic stem/progenitor cells (HSPCs) and erythroid progenitors downstream of stem cell factor (SCF) and erythropoietin (Epo) stimulation during regenerative erythropoiesis [1,2]. Samd14 shares homology with neurabin proteins (PPP1R9A and PPP1R9B), which promote cell signaling and survival in neurons [3]. Neurabin mechanisms of action include signaling complex recruitment to actin filaments and controlling specificity of signaling pathway activation within certain cell subtypes [4,5]. (Source: Experimental Hematology)
Source: Experimental Hematology - September 16, 2023 Category: Hematology Authors: Meg A. Schaefer, Pooja Roy, Srinivas Chava, Ainsley Meyerson, Andrew L. Duncan, Linda Chee, Kyle J. Hewitt Tags: Article Source Type: research
Physiological and Regenerative Functions of Sterile Alpha Motif Protein-14 in Hematopoiesis
Samd14 promotes signal pathway duration and intensity in hematopoietic stem/progenitor cells (HSPC) and erythroid progenitors downstream of stem cell factor (SCF) and erythropoietin (Epo) stimulation during regenerative erythropoiesis (1,2). Samd14 shares homology with neurabin proteins (PPP1R9A and PPP1R9B) which promote cell signaling and survival in neurons (3). Neurabin mechanisms-of-action include signaling complex recruitment to actin filaments and controlling specificity of signaling pathway activation within certain cell subtypes (4,5). (Source: Experimental Hematology)
Source: Experimental Hematology - September 16, 2023 Category: Hematology Authors: Meg A. Schaefer, Pooja Roy, Srinivas Chava, Ainsley Meyerson, Andrew L. Duncan, Linda Chee, Kyle J. Hewitt Tags: Article Source Type: research
Chronic Inflammation Promotes Cancer Progression as a Second hit
Acute myeloid leukemia (AML) is an aggressive hematologic malignancy with fast clinical progression and poor prognosis. It is characterized by the expansion of hyperproliferative and dysfunctional myeloid precursors that result from the gradual acquisition of two recurrent driver mutations that provide leukemogenic potential to the cell, as described by the “two-hit” theory [1]. Although each of these mutations alone does not cause leukemic transformation, the co-occurrence of specific abnormalities directly leads to AML development. (Source: Experimental Hematology)
Source: Experimental Hematology - September 12, 2023 Category: Hematology Authors: Monika Burocziova, Srdjan Grusanovic, Karolina Vanickova, Sladjana Kosanovic, Meritxell Alberich-Jorda Tags: Brief Communication Source Type: research
Chronic inflammation promotes cancer progression in murine models
Acute myeloid leukemia (AML) is an aggressive hematologic malignancy with fast clinical progression and poor prognosis. It is characterized by the expansion of hyperproliferative and dysfunctional myeloid precursors which result from the gradual acquisition of two recurrent driver mutations that provide leukemogenic potential to the cell, as described by the “two-hit” theory1. Even though each of these mutations alone does not cause leukemic transformation, the co-occurrence of specific abnormalities directly leads to AML development. (Source: Experimental Hematology)
Source: Experimental Hematology - September 12, 2023 Category: Hematology Authors: Monika Burocziova, Srdjan Grusanovic, Karolina Vanickova, Sladjana Kosanovic, Meritxell Alberich-Jorda Source Type: research
Corrigendum to ‘CCL8 deficiency in the host abrogates early mortality of acute graft-versus-host disease in mice with dysregulated IL-6 expression’ [Experimental Hematology 2022; 106: 47-57]
In the original article, the name of the 2nd author, Dr. Norio Takei, was not included. The correct Author line is shown above. (Source: Experimental Hematology)
Source: Experimental Hematology - September 7, 2023 Category: Hematology Authors: Keita Igarashi, Norio Takei, Tsukasa Hori, Masaki Yamamoto, Hitoshi Sohma, Nobuhiro Suzuki, Hiroyuki Tsutsumi, Yukihiko Kawasaki, Yasuo Kokai Tags: Corrigendum Source Type: research
